2710
T3D2668
Risedronate
Risedronate is only found in individuals that have used or taken this drug. It is a bisphosphonate used to strengthen bone, treat or prevent osteoporosis, and treat Paget's disease of bone.The action of risedronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Risedronate also targets farnesyl pyrophosphate (FPP) synthase. Nitrogen-containing bisphosphonates (such as pamidronate, alendronate, risedronate, ibandronate and zoledronate) appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass.
105462-24-6
5245
C7H11NO7P2
283.001080
White powder.
1.04e+01 g/L
Rapid absorption (~1 hr) after an oral dose, occurs throughout the upper gastrointestinal tract
The action of risedronate on bone tissue is based partly on its affinity for hydroxyapatite, which is part of the mineral matrix of bone. Risedronate also targets farnesyl pyrophosphate (FPP) synthase. Nitrogen-containing bisphosphonates (such as pamidronate, alendronate, risedronate, ibandronate and zoledronate) appear to act as analogues of isoprenoid diphosphate lipids, thereby inhibiting FPP synthase, an enzyme in the mevalonate pathway. Inhibition of this enzyme in osteoclasts prevents the biosynthesis of isoprenoid lipids (FPP and GGPP) that are essential for the post-translational farnesylation and geranylgeranylation of small GTPase signalling proteins. This activity inhibits osteoclast activity and reduces bone resorption and turnover. In postmenopausal women, it reduces the elevated rate of bone turnover, leading to, on average, a net gain in bone mass.
No evidence found for metabolization of risedronate in humans or mammals.
Route of Elimination: Risedronate is excreted unchanged primarily via the kidney. Insignificant amounts (<0.1% of intravenous dose) of drug are excreted in the bile in rats.
Half Life: 1.5 hours
No indication of carcinogenicity to humans (not listed by IARC).
For the treatment of Paget's disease of the bone (osteitis deformans), postmenopausal and glucocorticoid-induced osteoporosis
Side effects include abdominal pain, anxiety, back pain, belching, bladder irritation, bone disorders and pain, bronchitis, bursitis, cataracts, chest pain, colitis, constipation, depression, diarrhea, difficulty breathing, dizziness, dry eyes, eye infection, flu-like symptoms, gas, headache, high blood pressure, infection, insomnia, itching, joint disorders and pain, leg cramps, muscle pain, muscle weakness, nausea, neck pain, nerve pain, pain, pneumonia, rash, ringing in ears, sinus problems, sore throat, stomach bleeding, stuffy or runny nose, swelling, tendon problems, tumor, ulcers, urinary tract infection, vertigo, vision problems, and weakness.
2009-07-15T20:44:10Z
2014-12-24T20:25:48Z
Risedronate
C08233
183772
RISEDRONATE
Risedronic acid
DB00884
RIS
true
OC(CC1=CN=CC=C1)(P(O)(O)=O)P(O)(O)=O
C7H11NO7P2
InChI=1S/C7H11NO7P2/c9-7(16(10,11)12,17(13,14)15)4-6-2-1-3-8-5-6/h1-3,5,9H,4H2,(H2,10,11,12)(H2,13,14,15)
InChIKey=IIDJRNMFWXDHID-UHFFFAOYSA-N
283.1123
283.001074735
Exogenous
Solid
-3.6
HMDB15022
CHEMBL923
5055
<p>Srinivasa Rao V.N Divvela, Lenin Racha, Sivakumaran Meenakshisunderam, Ramesh Dandala, “Process for the preparation of risedronate sodium hemi-pentahydrate.” U.S. Patent US20070173484, issued July 26, 2007.</p>